Nogo receptor-vimentin interaction: a novel mechanism for the invasive activity of glioblastoma multiforme

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dc.contributor.authorY H Kang-
dc.contributor.authorS R Han-
dc.contributor.authorH Jeon-
dc.contributor.authorS Lee-
dc.contributor.authorJ Lee-
dc.contributor.authorS M Yoo-
dc.contributor.authorJ B Park-
dc.contributor.authorM J Park-
dc.contributor.authorJong-Tae Kim-
dc.contributor.authorHee Gu Lee-
dc.contributor.authorM S Lee-
dc.contributor.authorS H Lee-
dc.date.accessioned2020-02-07T16:30:18Z-
dc.date.available2020-02-07T16:30:18Z-
dc.date.issued2019-
dc.identifier.issnI000-0028-
dc.identifier.uri10.1038/s12276-019-0332-1ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/19091-
dc.description.abstractNogo receptor (NgR) has been shown to inhibit the migration and invasion of human glioma cells. However, little is known regarding the regulatory mechanisms of NgR in glioblastoma multiforme (GBM). In this study, we propose a novel mechanism that regulates the maturation process of NgR through an interaction with vimentin. The inhibition of TGFβ1 activity by LY2109761 attenuated the migration/invasion of GBM cells by upregulating cell-surface NgR. Conversely, the treatment of GBM cells with TGFβ1 suppressed NgR maturation. We showed that NgR and vimentin interact, which could be a possible mechanism for the suppression of NgR maturation. The knockdown of vimentin suppressed the migration/invasion of GBM cells through the increased maturation of NgR. Finally, TCGA (The Cancer Genome Atlas) analysis also supported the association of NgR and vimentin. The maturation of NgR is regulated by the interaction of vimentin and NgR, which attenuates the invasive activity of GBM, and might be a potential therapeutic target for brain cancer.-
dc.publisherSpringer-Nature Pub Group-
dc.titleNogo receptor-vimentin interaction: a novel mechanism for the invasive activity of glioblastoma multiforme-
dc.title.alternativeNogo receptor-vimentin interaction: a novel mechanism for the invasive activity of glioblastoma multiforme-
dc.typeArticle-
dc.citation.titleExperimental and Molecular Medicine-
dc.citation.number10-
dc.citation.endPage125-
dc.citation.startPage125-
dc.citation.volume51-
dc.contributor.affiliatedAuthorJong-Tae Kim-
dc.contributor.affiliatedAuthorHee Gu Lee-
dc.contributor.alternativeName강윤희-
dc.contributor.alternativeName한승로-
dc.contributor.alternativeName전형택-
dc.contributor.alternativeName이수혁-
dc.contributor.alternativeName이지수-
dc.contributor.alternativeName유승민-
dc.contributor.alternativeName박종배-
dc.contributor.alternativeName박명진-
dc.contributor.alternativeName김종태-
dc.contributor.alternativeName이희구-
dc.contributor.alternativeName이명신-
dc.contributor.alternativeName이승훈-
dc.identifier.bibliographicCitationExperimental and Molecular Medicine, vol. 51, no. 10, pp. 125-125-
dc.identifier.doi10.1038/s12276-019-0332-1-
dc.description.journalClassY-
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Division of A.I. & Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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